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Published February 1999 | public
Journal Article

Profilin and the Abl Tyrosine Kinase Are Required for Motor Axon Outgrowth in the Drosophila Embryo


The ability of neuronal growth cones to be guided by extracellular cues requires intimate communication between signal transduction systems and the dynamic actin-based cytoskeleton at the leading edge. Profilin, a small, actin-binding protein, has been proposed to be a regulator of the cell motility machinery at leading edge membranes. However, its requirement in the developing nervous system has been unknown. Profilin associates with members of the Enabled family of proteins, suggesting that Profilin might link Abl function to the cytoskeleton. Here, genetic analysis in Drosophila is used to demonstrate that mutations in Profilin (chickadee) and Abl (abl) display an identical growth cone arrest phenotype for axons of intersegmental nerve b (ISNb). Moreover, the phenotype of a double mutant suggests that these components function together to control axonal outgrowth.

Additional Information

© 1999 Cell Press. Received December 4, 1998; revised January 18, 1999. We thank Lynn Cooley and Esther Verheyen for sharing information and reagents prior to publication and Douglas Knipple and Ross MacIntyre for genomic clones in the 26A region. We thank the Drosophila Genome Center (supported by the National Institutes of Health Genome Center and the Howard Hughes Medical Institute) for the l(2)5205 P insertion line. We also thank the Drosophila stock centers (the Drosophila Stock Center at the University of Indiana and the Mid-American Drosophila Stock Center at Bowling Green State University) for a variety of genetic strains used in these experiments. D. V. V. is supported by a McKnight Scholar Award, a Klingenstein Fellowship, the Council for Tobacco Research, and National Institutes of Health grant NS35909. Z. W. is a National Eye Foundation Predoctoral Fellow. C. S. G. is an Investigator with the Howard Hughes Medical Institute.

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